Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Transcriptomics response to miR-644 overexpression in three breast cancer cell lines

ABSTRACT: The goal of the study is to investigate the effect of microRNA-644 overexpression by chemical mimics on gene expression in breast cancer cell lines. To this purpose control and microRNA-644 mimics are used to transfect MDA-MB-231 cells, SK-BR-3 cells, and MCF-7 cells respectively. Transcriptomics profiling was performed with Illumina HumanHT-12 V4.0 BeadChip microarray. Three cell lines are treated with scramble microRNA mimic (control herein) and microRNA-644 mimic (miR-644 herein), with two replicates per condition. mRNA expression is compared between miR-644 and control treatment within each cell line, respectively.

ORGANISM(S): Homo sapiens

SUBMITTER: Jitao David Zhang

PROVIDER: E-GEOD-82058 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

The miR-644a/CTBP1/p53 axis suppresses drug resistance by simultaneous inhibition of cell survival and epithelial-mesenchymal transition in breast cancer.

Raza Umar U Saatci Özge Ö Uhlmann Stefan S Ansari Suhail A SA Eyüpoğlu Erol E Yurdusev Emre E Mutlu Merve M Ersan Pelin Gülizar PG Altundağ Mustafa Kadri MK Zhang Jitao David JD Doğan Hayriye Tatlı HT Güler Gülnur G Şahin Özgür Ö

Oncotarget 20160801 31

Tumor cells develop drug resistance which leads to recurrence and distant metastasis. MicroRNAs are key regulators of tumor pathogenesis; however, little is known whether they can sensitize cells and block metastasis simultaneously. Here, we report miR-644a as a novel inhibitor of both cell survival and EMT whereby acting as pleiotropic therapy-sensitizer in breast cancer. We showed that both miR-644a expression and its gene signature are associated with tumor progression and distant metastasis- ...[more]

PMID: 27409664

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Project description:Withaferin A isolated from Withania somnifera (Ashwagandha) has recently become an attractive phytochemical under investigation in various preclinical studies for treatment of different cancer types. In the present study, a comparative pathway-based transcriptome analysis was applied in epithelial-like MCF-7 and triple negative mesenchymal MDA-MB-231 breast cancer cells exposed to concentrations of Withaferin A (WA) which can be detected systemically in in vivo experiments. Whereas WA revealed attenuation of multiple cancer hallmarks the withanolide analogue Withanone (WN), did not exert any of the described effects in these cells at comparable concentrations. Pathway enrichment analysis identified that WA targeted relevant cancer programs related to cell death, cell cycle and proliferation, which could functionally be validated flow cytometrically and by real-time proliferation xCELLigence assay. With respect to cell motility, invasion and metastasis processes, WA was found to strongly decrease MDA-MB-231 invasion as determined by single-cell collagen invasion assay. This is further supported by gene expression changes which demonstrate increased expression of a validated breast cancer metastasis suppressor gene (BRMS1) and concomitant decreased expression of extracellular matrix-degrading proteases (PLAU, PLAT, ADAM8), cell adhesion molecules (integrins, laminins) as well as pro-inflammatory mediators of the metastasis-promoting tumor microenvironment (TNFSF12, IL6, ANGPTL2, CSF1R). Subsequent in silico network analysis listed key node transcription factors regulating these processes (p53, E2F1, CDKN2A, NRF2) and revealed the role of chromatin modifying enzymes (p300, JARID1B) as central master switches, linking multiple anticancer activities of WA. Furthermore, hierarchical clustering analysis of 84 chromatin writer-reader-eraser enzymes revealed that WA treatment of invasive mesenchymal MDA-MB-231 cells reprogrammed their transcription levels more similarly towards the pattern observed in non-invasive MCF-7 cells. In conclusion, taking in account that sub-cytotoxic concentrations of WA target multiple metastatic effectors in therapy resistant triple negative breast cancer, WA based therapeutic strategies hold promise for further (pre)clinical development to defeat aggressive metastatic breast cancer. Total RNA from 2 different cell lines treated with WA, are compared to their untreated states

Dataset Information

Transcriptomics response to miR-644 overexpression in three breast cancer cell lines

Publications

The miR-644a/CTBP1/p53 axis suppresses drug resistance by simultaneous inhibition of cell survival and epithelial-mesenchymal transition in breast cancer.

Similar Datasets

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